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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96

Obesity is a well-known cause of upper airway narrowing, respiratory failure and resulting hypoxemia and hypercapnia, and cardiac arrhythmias during sleep. Obese patients are prone to snore loudly and to develop obstructive sleep apnea syndrome and also obesity-hypoventilation syndrome. Repeated nocturnal upper airway obstruction may cause respiratory failure and cor pulmonale and frequent awakenings, and result in nocturnal choking, with daytime drowsiness, somnolence and irritability. The purpose of this article is to review the evidence for these accepted facts and to consider a variety of new information that relates to the pathogenesis, symptomatology and treatment of sleep disorders caused by obesity.
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PMID:Sleep-related Disorders in the Obese. 1076 3

Daytime complaints like fatigue, sleepiness and cognitive dysfunction in neuromuscular disease can be due to nocturnal hypercapnia and hypoxemia. Daytime respiratory diagnostics does not reflect sleep disordered breathing. Nocturnal pulse oxymetry and capnography were performed in 11 patients (15-75 years old) with different slowly progressive neuromuscular diseases. Only four patients complained of dyspnea. Pulmonary function was abnormal in three patients. Blood gas samples showed a hypoxemia in three patients. Pulse oxymetry results were pathological in six patients. Nine patients presented abnormal capnographies. According to these results either nocturnal oxygen application was initiated or ventilatory parameters were modified. Daytime symptoms and muscular strength improved markedly. Capnography and pulse oxymetry should be performed during the course of neuromuscular disease to detect respiratory insufficiency. Capnography seems to be a more sensitive indicator for respiratory impairment especially when artificial ventilation has been initiated.
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PMID:Respiratory monitoring in neuromuscular disease - capnography as an additional tool? 1151 50

Obstructive sleep apnoea is a disease of increasing importance because of its neurocognitive and cardiovascular sequelae. Abnormalities in the anatomy of the pharynx, the physiology of the upper airway muscle dilator, and the stability of ventilatory control are important causes of repetitive pharyngeal collapse during sleep. Obstructive sleep apnoea can be diagnosed on the basis of characteristic history (snoring, daytime sleepiness) and physical examination (increased neck circumference), but overnight polysomnography is needed to confirm presence of the disorder. Repetitive pharyngeal collapse causes recurrent arousals from sleep, leading to sleepiness and increased risk of motor vehicle and occupational accidents. The surges in hypoxaemia, hypercapnia, and catecholamine associated with this disorder have now been implicated in development of hypertension, but the association between obstructive sleep apnoea and myocardial infarction, stroke, and congestive heart failure is not proven. Continuous positive airway pressure, the treatment of choice for obstructive sleep apnoea, reduces sleepiness and improves hypertension.
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PMID:Obstructive sleep apnoea. 1250 19

Prader-Willi syndrome (PWS) is a genetic disorder, with hypotonia being the predominant feature in infancy, and developmental delay, obesity, and behavioral problems becoming more prominent in childhood and adolescence. Children with this disorder frequently suffer from excessive daytime sleepiness and have a primary abnormality of the circadian rhythm of rapid eye movement sleep. They also have primary abnormal ventilatory responses to hypoxia and hypercapnia, and these abnormalities may be exacerbated by obesity. Children with PWS are at risk of a variety of abnormalities of breathing during sleep, including obstructive sleep apnea and sleep-related alveolar hypoventilation. Clinical evaluation should include a careful history of sleep-related symptoms and assessment of the upper airway and lung function. Polysomnography should be considered for those with symptoms suggestive of sleep-disordered breathing. Treatment options depend on the underlying problem, but may include behavioral interventions, weight control, adenotonsillectomy, and nocturnal ventilation.
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PMID:Sleep and breathing in Prader-Willi syndrome. 1220 50

Acute confusional syndrome, or delirium, is a transitory mental state characterized by the fluctuating alteration of awareness and attention levels. We present the case of a patient with acute confusional syndrome associated with obstructive sleep apnea syndrome (OSAS) aggravated by metabolic acidosis induced by oral acetazolamide treatment.A 70-year-old man with no history of neurological disease was referred with a clinical picture consistent with acute confusional syndrome presenting between midnight and dawn. During the admission examination infectious, toxic, and neurologic causes, or those related to metabolic or heart disease were ruled out. Arterial blood gases measured during one of the nighttime episodes of acute confusional syndrome showed mild hypoxia and hypercapnia with mixed acidosis. Signs and symptoms suggestive of OSAS had been developing over the months prior to admission, with snoring, sleep apnea, and moderate daytime drowsiness. Polysomnography demonstrated severe OSAS with an apnea-hypopnea index of 38. Mean arterial oxygen saturation was 83%; time oxygen saturation remained below 90% was 44%. The attending physician ordered the withdrawal of oral acetazolamide, which was considered the cause of the metabolic component of acidosis. Treatment with continuous positive airway pressure was initiated at 9 cm H2O, after a titration polysomnographic study. The patient continued to improve.OSAS, for which very effective treatment is available, should be included among diseases that may trigger acute confusional syndrome.
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PMID:[Acute confusional syndrome associated with obstructive sleep apnea aggravated by acidosis secondary to oral acetazolamide treatment]. 1516 96

Permanent tracheotomy was the first surgical procedure proposed for the treatment of severe obstructive sleep apnoea syndrome and is still the only surgical option that ensures, even in very severe cases, complete elimination of apnoea and, in turn, clinical remission. Improved knowledge of the causes of obstructive sleep apnoea syndromes and the increasing therapeutic options (instrumental, medical and surgical) have resulted in cases requiring tracheotomy as the only indispensable therapeutic option becoming more rare. At present, the only indications are in very occasional conditions of life-threatening obstructive sleep apnoea syndromes and in patients on whom continuous positive airway pressure is not tolerated or is not effective (severe deoxygenation or hypercapnia, severe respiratory disorder index, severe obstructive sleep apnoea syndrome-related arrhythmias, severe excessive daytime sleepiness, heart diseases or ischaemic encephalopathy exacerbated by obstructive sleep apnoea syndromes, obstructive pneumopathy exacerbated by obstructive sleep apnoea syndromes, severe obstructive sleep apnoea syndromes with few chances of resolution with other surgical procedures or failure of the latter). Moreover, it is the only therapeutic solution in rare nocturnal laryngeal stridor due to multisystemic atrophy (in which obstructive sleep apnoea syndrome is due to nocturnal laryngospasm of neurologic origin). Therapeutic tracheotomy must be permanent (tracheostomy) and, therefore, preferably carried out with a specific technique (skin-lined tracheotomy), able to guarantee greater stability, less risk of granulation tissue, wider opening of the tracheostomy, sufficient reversibility. In our experience, very few patients (10 cases) withsleep disorder breathing have been submitted to skin-lined tracheotomy. Of these, the majority were submitted to surgery for severe apnoea due to nocturnal laryngospasm on account of multisystemic atrophy (n = 7), while only 3 cases of obstructive sleep apnoea syndromes were submitted to skin-lined tracheotomy, i.e., 0.7% of the 424 patients operated on for obstructive sleep apnoea syndrome and 1.7% of the 175 operated on for severe, or very severe, obstructive sleep apnoea syndromes (RDI > 40). Skin-lined tracheotomy was not followed by important complications and expected results were achieved with immediate disappearance of daytime symptoms and considerable improvement in nocturnal apnoea. Besides sleep-related disorders, numerous clinical situations with indications for a permanent tracheotomy may benefit from the skinlined technique, such as severe laryngeal or tracheal stenoses, laryngeal diplegias, miasthenia gravis, lateral amyotrophic sclerosis, intractable aspiration, severe emphysema.
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PMID:Role of skin-lined tracheotomy in obstructive sleep apnoea syndrome: personal experience. 1546 94

Positive airway pressure (PAP) devices are used to treat patients with sleep related breathing disorders (SRBD) including obstructive sleep apnea (OSA). Currently, PAP devices come in three forms: (1) continuous positive airway pressure (CPAP), (2) bilevel positive airway pressure (BPAP), and (3) automatic self-adjusting positive airway pressure (APAP). After a patient is diagnosed with OSA, the current standard of practice involves performing full, attended polysomnography during which positive pressure is adjusted to determine optimal pressure for maintaining airway patency. This titration is used to find a fixed single pressure for subsequent nightly usage. A task force of the Standards of Practice Committee of the American Academy of Sleep Medicine reviewed the available literature. Based on this review, the Standards of Practice Committee developed these practice parameters as a guideline for using CPAP and BPAP appropriately (an earlier review and practice parameters for APAP was published in 2002). Major conclusions and current recommendations are as follows: 1) A diagnosis of OSA must be established by an acceptable method. 2) CPAP is effective for treating OSA. 3) Full-night, attended studies performed in the laboratory are the preferred approach for titration to determine optimal pressure; however, split-night, diagnostic-titration studies are usually adequate. 4) CPAP usage should be monitored objectively to help assure utilization. 5) Initial CPAP follow-up is recommended during the first few weeks to establish utilization pattern and provide remediation if needed. 6) Longer-term follow-up is recommended yearly or as needed to address mask, machine, or usage problems. 7) Heated humidification and a systematic educational program are recommended to improve CPAP utilization. 8) Some functional outcomes such as subjective sleepiness improve with positive pressure treatment in patients with OSA. 9) CPAP and BPAP therapy are safe; side effects and adverse events are mainly minor and reversible. 10) BPAP may be useful in treating some forms of restrictive lung disease or hypoventilation syndromes associated with hypercapnia.
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PMID:Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. 1655 24

Obstructive sleep apnea syndrome is caused by upper airway collapse during inspiration, causing intermittent hypoxemia, hypercapnia, acidosis, sympathetic nervous system activation, and arousal from sleep. Nighttime blood pressure is higher, but unexpectedly, daytime hypertension occurs. The prevalence of hypertension is very high and the incidence of hypertension increases as the number of apneic and hypopneic events per hour rises. Obesity is a major predisposing factor for the development of obstructive sleep apnea. Daytime sleepiness, snoring, and breathing pauses are important symptoms to elicit from the patient or sleep partner. Resistant hypertension is an important clue. Overnight polysomnography is required for diagnosis. Weight loss, avoidance of nocturnal sedatives, cessation of evening alcohol ingestion, and avoidance of the supine position during sleep are initial therapeutic actions in mild obstructive sleep apnea syndrome. Continuous positive airway pressure is the treatment of choice for patients unable to find relief from lifestyle changes. Blood pressure modestly improves with treatment.
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PMID:Obstructive sleep apnea syndrome. 1702 91

Excessive diurnal somnolence (EDS) represents the major symptom of sleep apnea syndrome (SAS). It is mainly determined by sleep fragmentation due to repetitive arousals following the episodes of nocturnal apneas and it is aggravated by the associated hypoxemia/hypercapnia. The EDS related decreased vigilance has 3 types of consequences: psychological (decreased capability of attention and concentration, increased of the response time to stimuli, irritability), motor (physical performance impairment, automatic behaviour) and social (accidents, decreased working performance). EDS evaluation relies on non-instrumental and instrumental strategies which are comprehensively presented. The therapy of EDS implies causes recognition and treatment, optimization of sleep hygiene and psychological advise.
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PMID:[Excessive diurnal somnolence--causes, mechanisms, therapeutical approach]. 1706 12


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